Eosinophilia in premature infants: correlation with chronic lung disease

We attempted to clarify the possible pathophysiological significance of eosinophilia in bronchopulmonary dysplasia (BPD). The subjects studied were 17 premature infants, i.e. seven with respiratory distress syndrome (RDS) followed by bronchopulmonary dysplasia (the BPD group: four with stage IV and three with stage III BPD) and 10 infants without BPD (the non-BPD group), who comprised seven with RDS, two with meconium aspiration syndrome and one with transient tachypnea of the newborn. Peripheral eosinophil counts, the number of nuclei of eosinophils and serum eosinophilic cationic protein (ECP) levels, and ECP and polymorphonuclear leukocyte (PMN) elastase levels of intratracheal aspirates (TA) were determined once a week during the first 4 weeks of life. Peripheral eosinophil counts were higher in infants with BPD than those in the non-BPD group. Hypersegmented nuclei of peripheral eosinophils with more than four nuclei were more frequently present in the infants with BPD. A good correlation was observed between peripheral eosinophil counts and serum ECP levels. ECP levels of the TA in the infants with BPD were significantly elevated. There was a good correlation between ECP and PMN elastase levels of the TA. Lung tissue specimens of two infants of the BPD group, both of whom had patent ductus arteriosus (PDA), were obtained from the lower portion of the left lung when they underwent an operative procedure for PDA at 24 and 25 days of life, respectively. Immunohistochemical staining of eosinophil-derived granular major basic protein (MBP) was performed on the lung tissue specimens. Infiltration of a few MBP-staining eosinophils was observed on the specimens from both infants. Our results suggest that peripheral eosinophils in sick premature infants may be activated and appear to be correlated with the severity of BPD. Further studies will be needed to more clarify the physiological role of eosinophils in premature infants.     

Host defence lectins in preterm neonates

AIM: Deficiency in collectins is discussed as a risk factor for pulmonary and systemic infections in children and adults. The objective of this study was to determine serum concentrations of surfactant protein D (SP-D) and mannose-binding lectin (MBL) in preterm and term infants at birth. METHODS: 47 preterm infants below 32 wk gestational age (GA) and 19 healthy, term newborn infants at birth have been included in the study, and SP-D as well as MBL concentrations have been determined in umbilical cord blood samples using sandwich ELISA technique. In addition, SP-D concentrations were assessed in tracheal aspirates (TA) of 24 mechanically ventilated preterms and in infants without pulmonary complications before elective surgery. RESULTS: MBL serum concentrations were significantly lower in preterms <32 wk GA (756.7 ng/ml; 14.6-11 184 ng/ml) compared to term newborns (3168.9 ng/ml; 282.3-7679.5 ng/ml; p=0.005; median and range, respectively). Serum SP-D concentrations were significantly decreased in preterms between 28 and 32 wk GA (1.4 ng/ml; 0-4.6 ng/ml; n=26) compared to term infants (2.2 ng/ml; 1.2-3.3 ng/ml; p=0.05) and were found to positively correlate with history of antenatal corticosteroids and chorioamnionitis. SP-D concentrations in TA were increased in preterm infants between 28 and 32 wk GA with respiratory distress syndrome (RDS) (25.0 ng/ml; 0.9-44.7 ng/ml; n=12) compared to control subjects (6.6 ng/ml; 0.5-30.4 ng/ml; n=12) in contrast to extremely immature infants <28 wk GA suffering from RDS (4.4 ng/ml; 0.8-78.4 ng/ml; n=12). CONCLUSION: In preterm infants, significant changes occur in collectin umbilical cord blood concentrations and pulmonary SP-D levels. Functional aspects of these findings need to be addressed further.     

High expression of pulmonary proteinase-activated receptor 2 in acute and chronic lung injury in preterm infants

Proteinase-activated receptor 2 (PAR(2)), a G-protein-coupled receptor activated by serine proteinases such as trypsin, has been suggested to play an important role in inflammatory and fibroproliferative processes. In preterm infants, the development of bronchopulmonary dysplasia (BPD) is characterized by early pulmonary inflammation and subsequent interstitial fibrosis. High pulmonary trypsin-2 has been shown to be associated with the development of BPD. We studied the expression and distribution of PAR(2) and trypsin-2 by immunohistochemistry in autopsy lung specimens of fetuses (n = 10), of preterm infants who died of acute or prolonged respiratory distress syndrome (RDS) (n = 8 and n = 7, respectively) or BPD (n = 6), and of newborn infants without lung disease (n = 5) who served as controls. In prolonged RDS and BPD, PAR(2) immunoreactivity was significantly higher in bronchial epithelium when compared with infants without pulmonary pathology (p < 0.05 and p < 0.005, respectively). In alveolar epithelium, expression of PAR(2) was elevated in prolonged RDS when compared with newborn infants without pulmonary pathology (p < 0.05). Moreover, strong expression of PAR(2) was detected in myofibroblasts of thickened and fibrotic alveolar walls in prolonged RDS or BPD. Trypsin-2 was co-localized with PAR(2) in bronchoalveolar epithelium. These findings suggest that PAR(2), possibly activated by trypsin-2, may participate in inflammation and fibroproliferation associated with progression of RDS toward BPD in preterm infants.     

Plasma endothelin-1 like immunoreactivity levels in neonates

We attempted to determine the plasma endothelin-1-like immunoreactivity (ET-1) levels and to evaluate its physiological significance in 29 neonates: 5 with respiratory distress syndrome (RDS), 3 with transient tachypnoea of the newborn (TTN), 4 with neonatal asphyxia, 5 with bronchopulmonary dysplasia (BPD) following RDS, 7 healthy preterm infants and 5 healthy full-term infants. Plasma ET-1 levels in infants with RDS were significantly higher than those in healthy full-term infants through the 1st week of life. Plasma ET-1 levels in infants with neonatal asphyxia were high on the first 2 days of life and then gradually decreased to those of healthy full-term infants. Plasma levels in infants with TTN were the same as those in healthy full-term infants. Plasma ET-1 levels in infants with BPD were high when compared with those in healthy preterm infants during the first 2 months of life. This study showed that plasma levels were markedly elevated for a long time in the infants with respiratory distress. We speculate that plasma ET-1 may be a specific marker for pulmonary endothelium injury in infants with respiratory distress.     

Respiratory disease and early serum S100A12 changes in very premature infants

Aim: The role of granulocyte‐specific S100A12, a marker for inflammatory disorders, in newborn lung disease is unknown. We compared postnatal blood S100A12 concentrations against respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD). Methods: Blood samples from 92 newborns were collected on admission, 12 h, day 1, day 3–4 and day 7, and analysed for S100A12. IL‐8 and IL‐6 were assayed in 52 infants. Results: Infants with RDS were significantly more premature (median 27 vs. 34 weeks), more likely to receive antenatal corticosteroids (84% vs. 26%) and have lower neutrophil counts (median 2.4 vs. 3.8 × 10⁹/L) at admission. S100A12 levels peaked during the first day and were significantly lower in preterm infants with RDS compared to those without (median 250 vs. 616 ng/mL at 12 h, 281 vs. 828 ng/mL day 1, respectively). S100A12 levels were low among the 35 very preterm infants (24–29 week gestation) regardless of the presence of BPD (285 vs. 288 ng/mL on day 1). In comparison, IL‐8 and IL‐6 levels were not different between groups. Conclusion: Plasma S100A12 is low in infants with RDS, possibly because of gestationally related differences in neutrophil response or to the effects of antenatal corticosteroids. It is therefore not a useful marker of BPD development.     

Extracellular release of bactericidal/permeability-increasing protein in newborn infants

Upon activation, polymorphonuclear leucocytes (PMN) release bactericidal/permeability-increasing protein, (BPI) from their azurophil granules. BPI selectively binds to the lipopolysaccharide (LPS) on gram-negative bacteria and induces their death. This study examined plasma BPI concentration levels in healthy newborns and in newborns with clinical sepsis, and the ability of PMN from preterm and term infants to release BPI. We also studied the release of myeloperoxidase (MPO), and the surface expression of adhesion molecule CD11b on PMN. In infants with clinical sepsis, plasma BPI concentration was higher, 27.8 microg/L [8.6-883; median (range)] (n = 11), than in healthy term infants 8.9 microg/L (3.9-179) (n = 17), and in adults 7.3 microg/L (0.7 -18.4) (n = 15); p = 0.014, Kruskal-Wallis. In preterm infants (n = 8), the ability of PMN to release BPI in vitro after stimulation with PMA was 8.8, in term infants it was 15.9 (n = 29; p > 0.05 vs. preterm infants) and in adults 23.4 ng/10(6) PMN (n = 15; p = 0.024 and p > 0.05 vs. preterm and term infants, respectively). The corresponding values of MPO were 20.0 ng/10(6) (11.3-46.7) in preterms, 19.0 ng/10(6) (2.2-223.7) in terms, and 27.8 ng/10(6) (9.1-80.7) in adults; p = 0.67 between groups. In infants with clinical sepsis, CD11b level was higher, 292 RFU (234-403) than the basal CD11b expression levels in healthy newborn infants, 116 RFU (76-145); P = 0.0001. FMLP-stimulated PMN CD11b expressions in preterm cord blood, 1071 RFU (552-1286) and in term cord blood, 918 (567-1472) were on the same level, but lower than that in adult blood, 1592 (973-1946); p < 0.001, ANOVA. Our findings suggest that in preterm infants the ability to release BPI is lower than in adults and term infants. These findings suggest that premature neonates have an impaired ability to mobilize BPI, possibly contributing to their marked susceptibility to infections with Gram-negative bacteria.     

Cord blood Clara cell protein CC16 predicts the development of bronchopulmonary dysplasia

Clara cell protein (CC16) is an anti-inflammatory protein and a biomarker of pulmonary epithelial cells and alveolocapillary membrane injury in adults. We investigated whether low cord blood concentrations of CC16 are associated with the development of respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) in preterm infants and the relationship between CC16 and its pro-inflammatory counterpart, the secretory phospholipase A₂ (sPLA₂) enzyme. CC16 concentration, sPLA₂ activity and IL-6 concentration were measured in cord blood plasma from 79 preterm infants (25 controls, 37 infants who developed RDS and 17 infants who developed BPD). After adjustment for gestational age and Apgar score at 5 min, the CC16 concentration was lower in BPD infants than in preterm controls (p<0.01). sPLA₂ activity was similar in all groups and the IL-6 concentrations were increased in both RDS and BPD infants (p<0.01 and p<0.05, respectively, vs. controls). We conclude that low cord blood CC16 concentrations in preterm infants independently predict the development of BPD. Low CC16 levels may reflect early lung injury, which contributes to the severity of RDS and progress towards BPD. Future studies are needed to assess whether the early administration of recombinant human CC16 in preterm infants with low cord blood CC16 prevents the development of BPD. This study was supported by grant 920-03-083 from the Netherlands Organisation for Scientific Research (NWO).     

Low postnatal serum IGF-I levels are associated with bronchopulmonary dysplasia (BPD)

Aim: To characterize postnatal changes in serum insulin-like growth factor-1 (IGF-I) in relation to development of bronchopulmonary dysplasia (BPD) in very preterm infants. Methods: Longitudinal study of 108 infants with mean (SD) gestational age (GA) 27.2 (2.2) weeks. Weekly serum samples of IGF-I were analysed from birth until postmenstrual age (PMA) 36 weeks. Multivariate models were developed to identify independent predictors of BPD. Results: Postnatal mean IGF-I levels at postnatal day (PND) 3–21 were lower in infants with BPD compared with infants with no BPD (16 vs. 26 μg/L, p < 0.001). Longitudinal postnatal change in IGF-I levels (IGF-I regression coefficient (β)), PNDs 3–21, was lower in infants with BPD compared with infants with no BPD (0.28 vs. 0.97, p = 0.002) and mean IGF-I during PMA 30–33 weeks was lower in infants with BPD as compared with infants without BPD (22 vs. 29 μg/L, p < 0.001). In a binomial multiple regression model, lower GA, male gender and lower mean serum IGF-I levels during PND 3–21 were the most predictive risk factors associated with BPD (r² = 0.634, p < 0.001). Conclusion: Lower IGF-I concentrations during the first weeks after very preterm birth are associated with later development of BPD.     

Connexin implication in the control of the murine beta-cell mass

Bronchopulmonary dysplasia (BPD) is a common adverse outcome of prematurity, causing severe morbidity and mortality. The cytokine macrophage migration inhibitory factor (MIF) has been recently shown to favor murine fetal lung development. In this prospective study, we evaluate the expression of MIF in the lung and in the serum of preterm infants (n = 50) and investigate whether the -173 G/C MIF promoter polymorphism is associated with the risk of BPD (n = 103). MIF was highly expressed in lung tissue from preterm infants. Serum MIF levels were measured by ELISA at d 1 after birth. MIF levels were increased [median (interquartile range), 71.01 (44.9-162.3) ng/mL], particularly in those infants with RDS [110.4 (59.4-239.2) ng/mL] compared with healthy adults [2.4 (1.2-5.0) ng/mL], (p < 0.001). The MIF -173*C allele, which predisposes to higher MIF production, was associated with a lower incidence of BPD (OR, 0.2; 95% CI, 0.04-0.93), independently from mechanical ventilation and oxygen exposure (p = 0.03). In conclusion, these data show that MIF expression is increased in lung and serum of preterm infants and suggest that the high producing MIF -173*C allele may be a protective factor for BPD.     

Increased eosinophil cationic protein levels in bronchoalveolar lavage from wheezy infants

Although studies examining the serum suggest a role for eosinophils in wheezing episodes in infants and toddlers, the presence of a chronic eosinophilic inflammation within their airways remains to be demonstrated. In this study we investigated whether eosinophil cationic protein (ECP) levels are increased in BAL fluid (BALF) from infants and toddlers with recurrent wheezing episodes, during an asymptomatic period. The levels of ECP in BALF were quantitated by radioimmunoassay in 61 children (36 with severe recurrent episodes of wheezing and 25 who were non-wheezy), aged 6–36 months, in whom flexible bronchoscopy was clinically indicated. BALF eosinophil counts were ≤ 1% in all patients and did not differ in wheezers, compared to non-wheezers. In contrast, ECP levels in BALF were ≥ 2.2 µg/l in 18 of 36 (50%) wheezy infants but in only three of 25 (12%) control infants (p < 0.01). Neutrophil counts were significantly higher in the wheezer group than in the non-wheezer group (8.1 × 10³ cells/ml vs. 3.0 × 10³ cells/ml). ECP levels in the BALF were not correlated with the absolute number of eosinophils ( r  = 0.03; p = 0.8) but were correlated with the absolute number of neutrophils ( r  = 0.54; p = 0.001). There was no association between high ECP levels in BALF and the atopic status of the wheezers. In conclusion, ECP levels are increased in BALF from young children with recurrent wheezing episodes, even during relatively quiescent periods, suggesting a chronic increased cell activation in the lower airways.     

Elevated type IV collagen in bronchoalveolar lavage fluid from infants with bronchopulmonary dysplasia

We measured the levels of type IV collagen and lipid peroxides in bronchoalveolar lavage fluid (BALF) from infants with respiratory distress syndrome (RDS) to determine the relationship to the development of bronchopulmonary dysplasia (BPD). We analyzed their levels between two groups, RDS infants who developed BPD (n = 8, BPD group) and those who did not (n = 11, RDS group). The levels of the type IV collagen in the BPD group were significantly higher than those in the RDS group at 3 and 7 days of age (p = 0.0024). In the BPD group, persistently increased levels of the type IV collagen were observed during the period up to 14 days of age. There was a positive relationship between the type IV collagen levels and polymorphonuclear leukocyte counts, and thiobarbituric acid-reactive substance levels in BALF. These results suggest that the increased type IV collagen levels in BALF of BPD infants may reflect pulmonary basement membrane damage and the involvement of oxygen metabolites in its process.     

Tracheal lavage and plasma fibronectin: relationship to respiratory distress syndrome and development of bronchopulmonary dysplasia

Plasma for fibronectin determinations was obtained from 39 neonates with uncomplicated respiratory distress syndrome (RDS) and from 15 infants with RDS who developed bronchopulmonary dysplasia (BPD). Tracheal lavage fibronectin and albumin concentrations were measured in 15 infants with RDS and 15 with BPD. Control plasma fibronectin values were obtained from 20 healthy preterm infants on days 1, 2, 3, 14, and 30 of life. Control tracheal lavage fibronectin and albumin concentrations were measured in 17 neonates of various gestational ages who required tracheal intubation for nonpulmonary indications. Mean plasma fibronectin concentrations from patients with RDS was 121 +/- 11 micrograms/ml on days 1, 2, and 3, versus control level of 163 +/- 12 micrograms/ml (P less than 0.01). Mean tracheal lavage fibronectin/albumin ratio was 3.8 +/- 0.6 ng per microgram of albumin on days 1 to 5 for infants with RDS, versus control level of 5.6 +/- 3.6 (P = NS). Tracheal lavage fibronectin/albumin ratio from patients with BPD was elevated at 16.3 +/- 5.0 ng fibronectin per microgram of albumin on days 14 to 21, and 23.6 +/- 7.4 on day 30 (P less than 0.05 versus control and and versus RDS days 1 to 10). Low plasma fibronectin concentrations early in RDS may contribute to the development of pulmonary capillary leak. High tracheal lavage fibronectin levels may foster the development of pulmonary fibrosis in patients with BPD.     

早产儿出生时血清25-羟维生素D水平与支气管肺发育不良的相关性

目的分析早产儿出生时血清25-羟维生素D[25(OH)D]水平与支气管肺发育不良(BPD)的关系。方法选取2014年1月至2016年12月入住NICU、出生胎龄34周的早产儿,按是否患BPD分为BPD组(41例)和对照组(219例),分析25(OH)D水平与BPD的关系。结果 BPD组血清25(OH)D水平显著低于对照组(37±17 nmol/L vs 47±20 nmol/L;P0.05);维生素D缺乏率显著高于对照组(90.2%vs 74.0%,P0.05)。血清25(OH)D水平与BPD发生率呈负相关(r=-0.201,P=0.001)。结论早产儿维生素D缺乏可能与BPD发病有关,但需多因素分析进一步证实。     

Cytokine gene polymorphisms in Italian preterm infants: association between interleukin-10 -1082 G/A polymorphism and respiratory distress syndrome

In this study, we determined the genotype frequencies of polymorphisms of cytokine genes and investigated their association with the risk of respiratory distress syndrome (RDS) in preterm infants. Genetic polymorphisms in the cytokines interleukin (IL)-10, IL-8, and tumor necrosis factor (TNF) alpha, were studied in 342 white Italian newborns (112 without RDS, 66 prematurely born with RDS, and 164 infants born at term who were included as healthy controls). The polymorphisms were analyzed by polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP). The IL-10 mRNA levels were analyzed according to genotype by quantitative real-time PCR (QRT-PCR) in Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCLs) of 42 full-term healthy infants. Logistic regression analysis demonstrated the risk of RDS to be significantly lower in preterm infants with an IL-10 -1082 GG/GA genotype than in those with an AA genotype [odds ratio (OR) = 0.48, 95% confidence interval (CI): 0.24-0.95, p = 0.03]. QRT-PCR analyses showed that the IL-10 mRNA levels were significantly higher in 27 IL-10 -1082 GG/GA carriers compared with 15 IL-10 -1082 AA carriers (p = 0.03). We conclude that the IL-10 -1082 GG/GA polymorphism may have a role in RDS development in premature infants.     

Pulmonary artery pressure in term and preterm neonates

Systolic pulmonary artery pressure (PAP) during the first 4 days after birth was determined in 41 healthy term and 46 preterm infants by measuring ductal Doppler flow velocity and systemic arterial pressure (SAP). Among preterm infants, 21 had respiratory distress syndrome (RDS) and 25 did not. Sequential indices within 96 h of age were presented respectively. At the ages of 2 and 12 h the ratio between pulmonary and systemic arterial pressure was significantly higher in term than in preterm infants without RDS ( p < 0.05). At the age of 24 h, PAP to SAP ratio was similar in all study groups. Between 48 and 72 h, PAP to SAP ratio was significantly higher in preterm infants with RDS than in infants without RDS ( p < 0.05). Our findings indicated that: (1) in healthy fullterm infants pulmonary artery pressure fell to subsystemic level during the first 12 h. indicating the critical time in circulatory transition; (2) prematurity did not affect ductal closure times significantly; and (3) RDS was associated with prolonged ductal patency and delayed postnatal circulatory adaptation characterized by pulmonary hypertension.     

外周血内皮祖细胞与极低出生体重早产儿并发症发生相关性

目的 分析内皮祖细胞（EPCs）与极低出生体重早产儿发生支气管肺发育不良（BPD）、早产儿视网膜病（ROP）和脑室内出血（IVH）并发症的相关性。方法 选取于复旦大学附属儿科医院NICU住院的胎龄<32周、出生体重<1 500 g的早产儿,分别于出生时、生后7、14、21和28 d及纠正胎龄36周时收集外周血,流式细胞仪检测EPCs水平,酶联免疫法检测血管内皮生长因子（VEGF）、基质细胞衍生因子等水平。结果 68例极低出生体重早产儿纳入分析,其中对照组30例,BPD 组20例, ROP组 10例,IVH组 8例。BPD组与对照组出生时EPCs水平差异无统计学意义,生后7 d时点EPCs水平较对照组明显降低,CD34+KDR+: (0.019 ±0.009) % vs (0.026±0.012)%, P<0.05; KDR+CD133+: (0.004±0.002)% vs (0.008±0.004)%, P<0.01; CD34+KDR+CD133+: (0.005±0.002)% vs (0.008±0.004)%, P<0.05。从出生时至生后21 d,BPD组血浆VEGF水平均明显低于对照组。ROP组出生时至生后28 d的EPCs水平与对照组差异无统计学意义,纠正胎龄36周时KDR+CD133+和CD34+KDR+CD133+ EPCs与对照组相比略有升高趋势。与对照组相比, IVH组生后不同时点的EPCs水平差异均无统计学意义。结论 生后早期的EPCs和VEGF水平降低可能参与了早产儿BPD的发生,但其具体机制仍需进一步研究。     

沐舒坦预防早产儿呼吸窘迫综合征的Meta分析

目的：系统评价沐舒坦预防早产儿呼吸窘迫综合征（respiratory distress syndrome,RDS）的有效性及安全性。方法：电子检索Cochrane图书馆、PubMED、EMBASE、中国生物医学文献数据库、中国期刊全文数据库、万方和维普数据库等,手工检索Pediatrics及Pediatric Research中刊载的会议论文。检索沐舒坦预防早产儿RDS的随机对照试验（randomized controlled trial,RCT）文献。应用Cochrane协作网推荐的方法评价文献质量,对同质研究采用RevMan 5.0.17软件进行Meta分析。结果：共纳入6个RCT,其中1篇质量评价为A级,1篇为B级,4篇为C级,包括823例早产儿。Meta分析结果显示,沐舒坦预防组与对照组比较,在RDS发病率(OR=0.24,95%CI［0.15,0.64］,P＜0.01)、支气管肺发育不良（BPD）发病率(OR=0.41,95%CI［0.23,0.75］,P<0.01)、脑室内出血（IVH）发病率(OR=0.39,95%CI［0.24,0.64］,P<0.01)、动脉导管未闭（PDA）发病率(OR=0.33,95%CI ［0.17,0.67］,P<0.01) 及肺部感染发病率(OR=0.24,95%CI［0.14,0.38］,P＜0.01)差异均有统计学意义。所有研究均未报道不良反应的发生。结论：现有证据表明,早产儿早期使用沐舒坦预防性治疗能有效减少RDS、BPD、IVH、PDA及肺部感染的发病率。［中国当代儿科杂志,2010,12（11）：858-863］     

High serum cardiac troponin T concentrations in preterm infants with respiratory distress syndrome

In preterm infants with respiratory distress syndrome (RDS), cardiac function is negatively influenced by the severity of the lung disease. On day 2 of life, cardiac troponin T (cTnT), biochemical marker of myocardial injury, was measured in 46 preterm infants (gestational age < or =32 wk), 26 with RDS and 20 without: median (range) 0.38 (0.02-1.57) microg/L vs 0.13 (0.02-0.85) microg/L, respectively. CONCLUSION: High cTnT concentrations in preterm infants with RDS suggest the presence of myocardial damage in this group of high-risk patients.     

Plasma carnitine levels in preterm infants with respiratory distress syndrome

BACKGROUND: Antenatal carnitine administration has been shown to induce fetal lung maturity by increasing pulmonary surfactant in animal and human studies. In this study, the aim was to investigate the status of carnitine in maternal and neonatal plasma of preterm infants with respiratory distress syndrome (RDS) in the first hours of life. METHODS: Maternal plasma carnitine levels were determined before delivery and neonatal plasma carnitine levels were determined within 2 h of birth in preterm infants (< 34 weeks gestational age) who developed RDS in the first 6 h of life and in the control group. RESULTS: The mean neonatal plasma free carnitine level was significantly lower in preterm infants with RDS than in the control group (28.3 +/- 8.8 micromol/L and 36.9 +/- 18.4 micromol/L, respectively; P < 0.05) while the mean maternal plasma-free carnitine levels were similar in both groups. CONCLUSIONS: Low neonatal plasma carnitine levels in preterm infants with RDS may be due to decreased maternal-fetal transfer of carnitine or to increased consumption of carnitine in fetal lung tissue for surfactant synthesis. This could be a contributing factor in the pathogenesis of respiratory distress syndrome in preterm infants.